School of Special Education and Rehabilitation, Binzhou Medical University, Yantai, Shandong, China.
Department of Rehabilitation, Binzhou Medical University Hospital, Binzhou, Shandong, China.
J Orthop Surg Res. 2024 Mar 25;19(1):198. doi: 10.1186/s13018-024-04676-1.
This study aimed to evaluate the protective effects of gentiopicroside against lipopolysaccharide-induced chondrocyte inflammation.
SW 1353 chondrosarcoma cells were stimulated with LPS (5 μg/ml) for 24 h and treated with different concentrations of gentiopicroside (GPS) for 24 h. The toxic effects of GPS on chondrocytes were determined using a CCK-8 assay and EdU staining. Western blotting, qPCR, and immunofluorescence analysis were used to examine the protective effect of GPS against the inflammatory response in chondrocytes induced by lipopolysaccharide (LPS). One-way ANOVA was used to compare the differences between the groups (significance level of 0.05).
The CCK-8 results showed that 10, 20 and 40 μM GPS had no significant toxic effects on chondrocytes; GPS effectively reduced the production of IL-1β and PGE2, reversed LPS-induced extracellular matrix degradation in cartilage by inhibiting the Stat3/Runx2 signaling pathway, and suppressed the hypertrophic transformation of SW 1353 chondrosarcoma cells.
Our study demonstrated that GPS significantly inhibited the LPS-induced inflammatory response and hypertrophic cellular degeneration in SW 1353 chondrosarcoma cells and is a valuable traditional Chinese medicine for the treatment of knee osteoarthritis.
本研究旨在评估龙胆苦苷对脂多糖诱导的软骨细胞炎症的保护作用。
用 LPS（5μg/ml）刺激 SW 1353 软骨肉瘤细胞 24 h，并用不同浓度的龙胆苦苷（GPS）处理 24 h。CCK-8 检测和 EdU 染色法测定 GPS 对软骨细胞的毒性作用。Western blot、qPCR 和免疫荧光分析用于检测 GPS 对脂多糖（LPS）诱导的软骨细胞炎症反应的保护作用。采用单因素方差分析比较组间差异（显著性水平为 0.05）。
CCK-8 结果表明，10、20 和 40 μM GPS 对软骨细胞无明显毒性作用；GPS 能有效降低 IL-1β 和 PGE2 的产生，通过抑制 Stat3/Runx2 信号通路逆转 LPS 诱导的软骨细胞外基质降解，并抑制 SW 1353 软骨肉瘤细胞的肥大转化。
本研究表明，GPS 能显著抑制 LPS 诱导的 SW 1353 软骨肉瘤细胞炎症反应和肥大性细胞退变，是治疗膝骨关节炎的一种有价值的中药。
